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Bernd Fritzsch, PhD

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Brief description of current research:

The development of the insulin-producing pancreatic beta-cells shows many molecular similarities with the inner ear sensory neurons, the main research area of my laboratory. Specifically, several transcription factors in the basic helix-loop-helix family and the LIM/homeodomain family play essential roles in cell fate determination and cell differentiation for both cell types. For example, the proneural gene Neurod1 has been independently cloned from the pancreas and was named Beta2. Deletion of this gene in mouse mutants causes loss of nearly all inner ear neurons and pancreatic beta-cells. Consistently, mutations in the human NEUROD1 gene are associated with maturity onset of diabetes of the young (MODY6), implying a critical role of Neurod1 in beta-cell maturation across species. We use genetically-engineered mouse mutants to study primarily inner ear neurosensory development and many of the mutations also affect pancreas development due to the similarities in gene regulation between these two developmental processes. Moreover, some of our mutants have even more profound effects in the pancreas owing to the differences in the regulatory complexity and the effectiveness of the transgenes. Currently we are investigating several novel mouse mutants that help us to further understand the molecular mechanism of both neurosensory and pancreas development and explore the potential use in regenerative medicine.